I. Field of the Invention:
This invention relates generally to biomedical apparatus; and more particularly to a system for detecting the onset of tachyarrhythmias, such as ventricular fibrillation whereby effective intervention can be initiated to restore the patient to normal sinus rhythm.
II. Discussion of the Prior Art:
To better comprehend the prior art, it is deemed necessary to explain the physiologic characteristics of the heart which might be used for distinguishing between normal sinus rhythm (SR), ventricular tachycardia (VT), supra-ventricular tachycardia (SVT) and ventricular fibrillation (VF). In SR, there is a synchronized depolarization of the cardiac cells resulting in the conventional QRS electrogram waveform. In VF, however, the cardiac cells generally lose their synchrony and the depolarization of one cell or group of cells no longer bears any particular relationship to the depolarization of other cell groupings resulting in a loss of distinct rhythm. Not only does the rhythm become indistinct but morphological changes also occur such that the beats are no longer of uniform shape due to the fact that the number of cells participating in each independent and nonsynchronized depolarization also changes.
Known VT and VF sensing techniques have involved the use of a bipolar or unipolar catheter disposed proximate the right ventricular apex for detecting signals occasioned by the cell depolarization and the use of a counting algorithm in an attempt to distinguish between SR, VT and VF on the basis of pulse rate. In connection with that algorithm, VF is considered to be a heart rate that is greater than some certain value typically exceeding rates associated with VT.
It is also found that the transition from SR to either VT or VF is generally accompanied by a fairly severe change in morphology or pulse shape because the overall pattern of depolarization and timing between cell changes when passing from SR through the onset of VT. A number of pulse counting techniques described in the literature depend not only upon determining the rate of the tachycardia, but also on the so-called "rate of onset". That is to say, they not only assess the absolute pulse rate but how rapidly the tachycardia begins relative to sinus rhythm. Investigators have determined that absolute rate alone is not a reliable indicator of VT or SVT in that high SR may be physiologically appropriate due to physical activity or even sudden fright resulting in autonomic stimulus to the heart. The "rate-of-onset measure" is generally based upon a threshold criteria determined by how rapidly the interval between successful QRS complexes is changing. Even when rate-of-onset considerations are relied upon in conjunction with absolute rate, known prior art detection apparatus still may mistake physiologically appropriate tachycardias from the non-appropriate tachycardias, i.e., there is an overlap in the domain which could contribute to inappropriate intervention. Moreover, pulse morphology changes have frequency extensions, as well, which may affect detection circuit performance. This may occur precisely at the critical point where rate-of-change information is needed for rate determination. Thus rhythm discrimination techniques which depend on rate and rate-of-change measurements may fail on two counts: rate overlap and misidentified rate changes.
Another known approach for identifying and discriminating the states and transitions between SR, SVT, VT and VF is based upon measurements on the cardiac electrogram and utilizes a frequency analysis technique which is used in determining the rhythm from the power spectrum. This technique is limited to the surface ECG by computational requirements. Still other techniques attempted for identifying and discriminating between normal SR and various tachycardias and fibrillation involve morphologic measures, such as rise time or polarity of the ECG waveform and the so-called "probability density function (PDF)" measurements in which the cardiac waveform is characterized by the relative percentage of time that it spends at various amplitude levels.
Each of these techniques has significant shortcomings. The outcome of the evaluation involving the PDF, for example, is found to be quite dependent upon electrode placement and the evaluation function requires an inordinate amount of time. Implantable tachyarrhythmia control devices have a variety of responses keyed to specific arrhythmias. The appropriate response is selected and triggered by the arrhythmia detection circuit. Inappropriate or missed detections carry significant penalties.
While maintaining accuracy, arrhythmia recognition, especially for VF, must be prompt. Shortening the interval from VF onset to intervention results generally in a higher proportion of successes due to halting the decay of the cardiac substrate before that process becomes irreversible. While it is not yet clear that this benefit extends to the first 30 seconds following onset, it is still vital that recognition, which controls the entire process leading to intervention, be as accurate and timely as possible. In the presence of SR and SVT, however, intervention is inappropriate. False identification of SR or SVT as VT or VF can lead to potentially dangerous intervention, again confirming the need for accuracy.
In contrast to the prior art, the present invention relies upon a spacial coherence detection approach to tachyarrhythmia discrimination. It was observed that the morphologic and probability density function techniques referred to above depended on a determination of the temporal departure from synchronization on a beat-to-beat basis. This, however, results from and is secondary to spacial decorrelation over the entire cardiac domain. It was felt that the temporal detector, based upon signals picked up by a single lead, would take an inordinate amount of time from the onset of VF or VT due to the degree of spacial desynchronization that must occur in order to appear locally on such a single lead. In the case of the present invention, a measurement is taken of the spacial decorrelation directly. Instead of using a single sensing electrode, one or more leads having plural electrodes are implanted within the heart but at somewhat remote locations with respect to one another, assuring that substantially distinct segments of cardiac tissue dominate the electrical field surrounding each electrode. As a result, the dominant electrical activity influencing one lead tends to be somewhat independent from the electrical activity influencing the other lead. During SR, each electrode receives some contribution from every electrically active cardiac cell. While the resulting QRS complex may appear quite different on the two leads, these signals are substantially coherent in the sense that there is a linear relationship between them. That is, QRS wave on one lead may be derived from that on the other via a linear transfer function. Assuming that the leads are mature and stable in the sense that they do not move, the transfer function also will be stable and will consistently reproduce the signal on one lead from that on the other.
During VT, the QRS morphology on both leads will, in general, appear different than during SR or SVT. This difference reflects the change in the depolarization sequence, as the depolarization wave travels through the muscle tissue, rather than the Purkinje fibers. In stable, monomorphic VT, the signals on the two leads will again be substantially coherent, but with different linear relationship than that which describes SR. Stated otherwise, a different transfer function is required to convert the signal on one lead to that of the other.
During VF, the depolarization sequence is constantly modifying from beat-to-beat, with dispersal of the depolarization sequence occurring to the point where cardiac activity can no longer be characterized as a sequence of beats, but rather as continuous, fragmented electrical activity.
The concept of coherence and the implied existence of linear transfer function depend on the existence of a persistent linear relationship. Taking the ratio of the complex spectra of the electrode signals over a specific time interval produces a result which resembles a transfer function, but does not carry with it the weight of persistence. Thus, such a function could be derived for every interval during the course of fibrillation, but the result would be inconsistent and incoherent. A stable transfer function cannot be said to exist under these circumstances. Thus, during VF, not only the signal morphology is changing, but the channel characteristics between leads, as reflected in the transfer function, is likewise changing.